Transport of anionic substrates and glutamate metabolism in mitochondria from ascites tumor cells.
A study is presented of alpha-oxoglutarate and glutamate transport and of glutamate oxidation in ascites tumor cell mitochondria. Kinetics analysis of alpha-oxoglutarate transport in mitochondria from two strains of Ehrlich ascites tumor cells, the hyperdiploid and the hyperdiploid Lettré mutant, shows that the activity of the alpha-oxoglutarate carrier and its affinityfor substrates are higher in the mutant than in the wild strain. Evidence is presented showing the occurrence of carrier mediated glutamate-OH-exchange-diffusion in mitochondria from both strains. The activity of the glutamate carrier is apparently higher in the hyperdiploid Lettré mutant. Glutamate oxidation occurs mainly through transamination to asparatate in both tumor stains. The rate of deamination in the two strains correlates directly with the level of glutamide dehydrogenase (EC 1.4.1.3.), which is higher in the wild than in the mutant strain. Thus glutamate dehydrogenase per se, and not glutamate penetration, constitutes the control step for gluttochondria of glutamate with externally added oxaloacetate (arsenite present) that exclude an obligatory transport of oxaloacetate on the alpha-oxoglutarate carrier.[1]References
- Transport of anionic substrates and glutamate metabolism in mitochondria from ascites tumor cells. Eboli, M.L., Paradies, G., Papa, S. Cancer Res. (1976) [Pubmed]
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